Am. J. Respir. Crit. Care Med., Volume 162, Number 1, July 2000, 216-220

Factor Analysis of Changes in Dyspnea and Lung Function Parameters after Bronchodilation in Chronic Obstructive Pulmonary Disease

CHRISTIAN TAUBE, BURGHART LEHNIGK, KIRSTEN PAASCH, DETLEF K. KIRSTEN, RUDOLF A. JÖRRES, and HELGO MAGNUSSEN

Institute for Pulmonology Research, Grosshansdorf Hospital, Center for Pulmonology and Thoracic Surgery, Grosshansdorf, Germany

Expiratory airway collapse is a characteristic feature in patients with chronic obstructive pulmonary disease (COPD). We hypothesized that this collapse might mask the effects of bronchodilators during forced expiration but not during forced inspiration, and that accordingly, the improvement in forced inspiration and not that in forced expiration with bronchodilator therapy would be related to changes in the perception of dyspnea. In order to investigate this, we conducted lung function measurements, including measurements of forced inspiration and expiration before and 30 min after inhalation of 400 µg salbutamol, in 61 patients with COPD (mean FEV₁: 38.3 L; range: 12.9 to 79.5% predicted). The change in dyspnea from baseline was assessed with a standard visual analogue scale (VAS) ranging from 100 to +100. To delineate the relationship between parameters, we used the statistical procedure of factor analysis. Salbutamol induced an improvement of 0.16 ± 0.02 L (mean ± SD) in FEV₁, 0.36 ± 0.04 L in forced inspiratory volume in one second (FIV₁), 0.30 ± 0.04 L in inspiratory capacity (IC), and 0.34 ± 0.07 L in intrathoracic gas volume; the mean VAS score was 36.4 ± 3.2. Factor analysis demonstrated that the reduction in dyspnea at rest was primarily associated with changes in parameters describing forced inspiration and not with those of forced expiration or lung hyperinflation, including IC. Our data indicate that in patients with COPD, the reduction in dyspnea after inhalation of a ₂-adrenoreceptor agonist is closely correlated with the change in parameters of forced inspiration, and particularly FIV₁, but not with changes in parameters of forced expiration or lung hyperinflation.

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